Cancer of the colon is the second most prevalent malignancy in the U.S. There is strong evidence that adenomatous colon polyps are precursor lesions of colon cancer. Such polyps are found in approximately 10% of adults, with incidence increasing to as high as 50% in persons over 70. it has recently been confirmed that certain nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit cyclooxygenase and the synthesis of prostaglandins, can reduce formation of both colon polyps and cancers in experimental animals given known carcinogens. NSAIDs have been reported to cause regression of adenomatous colon polyps in a small number of patients with familial polyposis and of desmoid tumors in persons with Gardner's syndrome. Most recently, the NSAID piroxicam effectively prevented development and progression of azoxymethane-induced colon cancer, even when administered as late as 13 weeks after carcinogen exposure. A clear dose- response relationship was convincingly demonstrated for piroxicam, with tumor suppression apparent at even the lowest dose tested. We have demonstrated that treatment with 20mg and 10mg piroxicam daily significantly reduces PGE2 content of rectal mucosa in patients with adenomatous colon polyps. Preliminary results suggest that even lower doses of piroxicam may significantly affect colon mucosa as reflected by suppression of PGE2 content. It will be important to determine whether the demonstrated short term effect of a low dose persists during prolonged therapy, whether patients will comply with such, and whether drug side effects occur at this low dose. The rationale for this proposed phase IIb study is derived from the demonstrated effectiveness of piroxicam in preventing colon cancer in animal models and the need to gain clinical experience with a different and lower dose of the drug than normally used in treatment of human disease, and to document that the dose employed causes a sustained effect on colon mucosa.